B cell antibody responses can be activated by helper T cells through two distinct pathways. Individual cloned T helper cell populations are in fact capable of mediating both MHC-restricted and non-MHC-restricted pathways of B cell activation. It was subsequently demonstrated that cloned lines of Lyt 1+ 2- L3T4+ antigen specific and MHC restricted suppressor cells can mediate suppressor effector function in these T dependent antibody responses. The role of T cells in regulating the fine specificity of B cell antibody responses was studied by examining the T15 idiotype dominant response to phosphocholine (PC) and the CRIA dominant response to Ars. It was found that cloned populations of carrier specific and MHC restricted T helper cells were capable of supporting T15 or CRIA idiotype dominant responses in B cells of appropriate haplotype. These findings demonstrated that no absolute requirement exists for the participation of idiotype specific TH2 cells in the generation of optimally idiotype dominant responses in this experimental system. A role of both specific and non specific T cell derived signals was demonstrated for activation of B cell antibody responses. It was shown that the supernatants of activated cloned T helper cells were capable of replacing these T cells in the antigen specific and MHC restricted induction of B cell IgG antibody responses. Two distinct and synergizing activities were identified in this supernatant: Interleukin 4, and an antigen-specific and MHC- restricted soluble factor. It was demonstrated that this latter factor can be affinity purified employing monoclonal antibodies specific for T cell receptor V-beta8 determinants. A mechanism for the rapid and directed secretion of mediators by T help was also demonstrated by analysis of granule exocytosis by T helper cells. Cloned helper cells, in response to T cell receptor mediated stimuli but not in response to IL2, rapidly secrete the contents of cytoplasmic granules. This provides a potential mechanism for the transmission of B cell activating stimuli from helper T cells to target B cells.